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Skeletal System
 Structure & Function
 Development & Growth
 Bone Homeostasis
 Osteoporosis & other
bone disorders
The evil that men do lives after them,
the good is oft interred with their bones.
—William Shakespeare (1564-1616)
Julius Caesar, Act III, Scene 2
A Bone’s Shape Makes Possible its Functions
• Shape & form
• Support
• Protection
• Movement
• Storage
• Hematopoiesis
Sites of muscle attachments
Bone Structure
 Structures of a long bone:
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periosteum: tough fibrous membrane covering
diaphysis: shaft - b/t epiphyses, long axis of bone
articular cartilage: portion of epiphysis covered w/ cartilage
epiphysis: expanded ends of bone -- proximal & distal
medullary cavity: hollow chamber w/in diaphysis, endosteum
membrane lines cavity & marrow resides w/in
– compact bone (cortical): near surface, continuous ECM w/ no
spaces -- dense & hard
– spongy bone (cancellous): w/in compact bone, consists of
network of thin strands of trabeculae
Gross Anatomy of a Long Bone
Cellular Structure of Bone
• Compact bone: cells, ECM & mineral salts form an
osteon
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contain blood vessels & nerves surrounded by CT
perforating canals transverse central canals
osteocytes lie in small concavities (lacunae) b/t lamellae
canaliculi - provide communication b/t osteocytes
• Spongy bone: cells & ECM lie w/in trabeculae
– no osteon or central canals – irregular lamellae & osteocytes
– trabeculae are formed where stress is exerted on the bone
– receive nutrients via diffusion from the canaliculi
Structural Unit of Compact Bone: Osteon
Lamella
Microscopic Structure of Spongy Bone
Gross Anatomy of a Long Bone
Principal Cells of Bone Tissue
Chemical Composition
of Bone
 Organic components:
– Cells: osteogenic, osteoblasts,
osteocytes & osteoclasts
– ECM: contribute to
structure & tensile strength
bone’s
 Inorganic components:
– mineral salts: calcium phosphate & carbonate which
account for bone’s hardness
Osteogenesis
 Intramembranous ossification (flat & irregular):
- originate as sheet-like layers of CT
- partially differentiated CT form into osteoblasts
- deposit bony matrix -- forming spongy bone
 Endochondral ossification (long & short):
- develop from hyaline cartilage -- model for bone formation
- CT covering cartilage becomes infiltrated w/ blood vessels
forming periosteum
- CT differentiates into osteoblasts forming spongy bone w/
ossification continuing deposition of compact bone occurs
Intramembranous Ossification
Stages in Endochondral Ossification
Occurring in a Long Bone
Endochondral
Ossification
Forming skeleton of an embryonic chicken, stained
with Alizarin Red and Alcian Blue to differentiate
between hardened bone (in red) and the remaining
cartilage model (in blue).
Bone Growth : elongation & appositional
Epiphyseal
Plate
http://highered.mcgraw-hill.com/classware/infoCenter.do?isbn=0072829532
X-ray Depicting Epiphyseal Plate
Osteoclasts & Medullary Cavity
 Multinucleated cells originate from WBC -- break down
calcified matrix (bone resorption):
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lysosomal enzymes digest organic components
acids secreted dissolve inorganic portion of matrix
phagocytes digest bony matrix
osteoblasts invade depositing new bone
 Formation of medullary cavity:
– primary ossification center enlarges -- osteoclasts break down
spongy bone
– cavity forms in center of diaphysis
– cavity fills w/ marrow, blood & lymph vessels & nerve fibers
• red & yellow marrow
Bone–Resorbing Osteoclast
Development of osteoblasts &osteoclasts
from bone marrow progenitors
Valsamis et al. Nutrition & Metabolism 2006 3:36
Homeostasis:
Bone Remodeling
 Continuous bone resorption
& bone deposition –
regulated via 2 control
loops:
1. negative feedback
(hormonal)
2. mechanical/gravitational
(Wolff’s law of bone)
Hormonal Control of Blood Ca++
• When Ca++ intake is  -blood [Ca++] are also 
• PTH stimulates osteoclasts
-- releasing Ca++ salts from
ECM into blood
• High intake blood [Ca++]
inhibits osteoclasts activity
• Calcitonin -- stimulates
osteoblasts activity,  bone
resorption & Ca++
excretion
(hypercalcemia)
(hypocalcemia)
Hormonal Control of Ca++ Balance
• Parathyroid hormone (PTH) – responsible for plasma [Ca++]
– mobilize Ca++ from bone ( bone resorption)
– enhances renal reabsorption of Ca++
– intestinal absorption of Ca++ (indirectly)
• Vitamin D3 – 1,25-dihydroxycholecalciferol (calcitriol):
– obtained from diet & sunlight
– supports effect of PTH – enhancing Ca++ uptake in small
intestine
– PTH & prolactin regulate production
• Calcitonin:
– released in association w/ plasma [Ca++]
–  bone resorption & renal excretion (action opposite to PTH)
Factors Affecting Bone Development,
Growth & Repair
 Nutrition: calcium, phosphorus, vitamins D, A, C & K
 UV radiation: dehydrocholesterol
 Hormones: hGH, T3 & T4, PTH and male & female
sex hormones
 Physical activity: weight bearing exercise & skeletal
muscle contraction (Wolff’s Law)
Fractures & Repair
• Fracture: classified by cause & nature of break (e.g.,
traumatic, compound)
– Blood vessels & periosteum rupture -- hematoma, swelling
& inflammation to surrounding tissue
– Angiogenesis: osteoblasts invade hematoma generating
spongy bone nearby & fibroblast produce fibrocartilage
(cartilaginous callus) and ECM
– Phagocytic cells remove blood clot & osteoclasts resorb
bone fragments
Key Steps in Repair of a Fracture
Types of Fractures
Rickets & Osteomalacia
• Pathology: failure of osteoid to calcify in a growing person,
most commonly assoc. w/ vitamin D deficiency in
hypocalcemia
• Signs & Symptoms: muscular hypotonia, thickening of
skull, softening of long bones (bowlegs), knobby deformity
in long bones & ribs, kyphoscoliosis
• Risk factors: dark skin, inner-city dwellers, breastfeed
infants w/o vitamin D supplementation
• Treatment: UV light, vitamin D, calcium & phosphorus
supplements,
Osteoporosis
• Pathology:  bone mass & mineral
content - w/in affected bones trabeculae
are lost -- spaces/canals enlarge filling
w/ fibrous & fatty tissues
• Signs & symptoms: bones fracture
easily (long bones), spontaneous breaks
- unable to support body weight
• Risk factors:  Ca++ & vitamin D
intake,  phys. act.,  estrogen levels,
cigarette smoking, alcohol abuse, medications: gender, age, body
size, ethnicity & genetics
• Screening & Treatment: DEXA; bisphosphonates; estrogen
therapy (ERT); PTH & exercise
Bone Mineral Acquisition
During Puberty
• Bone mineral density (BMD)
most rapidly b/t ages of 11-14 yrs
in girls & 14-17 yrs in boys
• Females reach 95% of adult BMD
by age 18 yrs & w/ only modest
gains up to 3rd decade of life
Gap in Ca++ Intake
• 86% of girls & 65% of boys aged
12-18 yrs fail to meet RDA of 1200
mg/d for Ca++
• Intake for Ca++ -- 1300 mg/d; gap
b/t the recommended & actual
intakes has widened
Barriers to Calcium Intake & Other Factors
Affecting Bone Mineral Density
• Ca++ content of common foods: http://www.nof.org/
• Meeting RDA of Ca++ is challenging when dairy products are not
consumed. Ca++ -fortified products offer a means of boosting Ca++
consumption through nondairy foods
• Nondairy sources of Ca++ such as breads, cereals, vegetables, and fish,
have a lower content or less bioavailable form. Ca++ -rich foods such as
DGLV, tofu, nuts, legumes & sardines are not part of the standard diet
• Inadequate vitamin D intake, lack of exposure to sunlight & reduced
vitamin D receptors in older adults all contribute
• Lack of phys. act., smoking, excessive alcohol consumption, diets Na &
phosphorus
Spinal Deviations of the Vertebral Column
Intervertebral Disc & Herniation
Carpal Tunnel Syndrome
• Pathology: swelling of tendons
reduces tunnel space -- squeezing &
injuring median nerve
• Symptoms: numbness, tingling,
pain, inflammation & clumsiness of
the hand
• Diagnosis & treatment: Tinel’s test, Phalen’s test, nerve conduction
velocity studies, patient history & occupational evaluation; antiinflammatory drugs, splints, avoidance of activities causing condition,
surgery and alternative therapies